Methodology: Adult female Wistar rats were time-mated and grouped into three categories: (a) control-given 0.1 mL of normal saline, (b) low-dose nicotine-given 6.88 mg/ kg/d/0.05 mL, and (c) high-dose nicotine-given 13.76 mg/kg/d/0.1 mL in two divided doses. Treatment was given intraperitoneally from gestational days 2 to 6. On postnatal day 15 (P15), the pups were separated from their mothers, anaesthetised and sacrificed, followed by intracardial perfusion with 4% paraformaldehyde. PFC was excised from the brain and processed for tissue histology, histochemistry, and morphology of brain cells.
Results: Gestational nicotine exposure during the first week of gestation in rats significantly reduced birth weights in nicotine-treated groups compared with control; it, however, accelerated body weights, altered neuronal morphology, and elevated astrocytic count significantly, while oligodendroglial count was slightly increased in the PFC of juvenile rats examined at P15.
Conclusion: These alterations revealed that gestational nicotine exposure before the commencement of the cellular processes involved in brain development negatively affects neurodevelopment, and this could result in neurological dysfunctions in later life.
Methods: A total of 63 unilateral nephrectomised male and female Wistar rats were divided into five groups. Group 1 (ShOPR): Rats as sham-operated group were subjected to surgical procedure without RIR. Group 2 (Isch): Rats underwent RIR (left kidney ischemia for 30 min followed by 48 h reperfusion). Group 3 (Zn+Isch): Rats were treated as group 2 but they received Zn sulphate (30 mg/kg) 1 h before induction of RIR. Group 4 (IPC+Isch): Rats were treated as group 2 but they underwent 1 min of ischemia followed by 3 min reperfusion as IPC, which was repeated for three times before induction of RIR. Group 5 (Zn+IPC+Isch): Rats were subjected to receive both Zn sulphate and IPC before induction of RIR. Urine samples were collected in the last 6 h of reperfusion, and finally biochemical and histological measurements were performed.
Results: The serum level of creatinine (Cr), normalised kidney weight (KW) and kidney tissue damage score (KTDS) increased by RIR alone significantly (P < 0.05). These parameters were attenuated statistically by Zn supplementation (P < 0.05). However, IPC alone or co-treatment of Zn and IPC did not improve the biochemical and histological markers altered by RIR injury.
Conclusion: Zn supplementation had a protective role against RIR while such protective effect was not observed by IPC alone or by co-treatment of Zn and IPC.
AIMS: To assess the estradiol induced changes in plasma ceruloplasmin concentration on exposure of the rats to acute stress.
SETTINGS AND DESIGN: Acute stress was induced by forcing the rats to swim till exhaustion. The rats were overiectomised bilaterally to remove the primary source of sex hormones. And hormone replacement was done later.
MATERIAL AND METHODS: Wistar albino female rats were used. Acute stress was induced before overiectomy, following recovery from surgery, and again after Estradiol Valerate injection (for 10 days) in same group of rats. The plasma ceruloplasmin was estimated immediately after stress during each stage--that is preoperative control, stressed control, after overiectomy and then following treatment with Estradiol Valerate.
STATISTICAL ANALYSIS USED: Paired sample T test was applied to analyze the findings.
RESULTS: We found lowest ceruloplasmin level after stress in overiectomised animals, while on substitution of estradiol the trend appeared to be reversed.
CONCLUSION: The result suggested a direct effect of estrogen on hepatic ceruloplasmin production/release and this could account for some of the beneficial effects of hormone replacement therapy.